A neurobiological explanation (dopamine hypothesis) Flashcards
what is a neurobiological explanation to schizophrenia?
The dopamine hypothesis
what’s the term for excess dopamine?
Hyperdopaminergia
Hyperdopaminergia AO1
Antipsychotic drugs chlorpromazine and haloperidol help symptoms of schizophrenia - but also induce side effects of tremors and muscle rigidity.
These are symptoms of Parkinson’s disease (low dopamine) - so schizophrenia was linked to high dopamine (hyperdopaminergia).
what two antipsychotic drugs help symptoms of schizophrenia?
chlorpromazine and reserpine
what are two explanation of why hyperdopaminergia may occur?
-Low levels of beta hydroxylase (enzyme that breaks down dopamine) may build up excess opine in synapses.
-Proliferation (rapid increase) of D2 dopamine receptors on postsynaptic cells due to hypersensitivity of a neurotransmitter may be responsible for hyperdopaminergic activity.
What’s the term for a dopamine deficiency?
hypodopaminergia
Hypodopaminergia AO1
-positive symptoms of schizophrenia (e.g delusions and hallucinations) may result from excess dopaminergic activity in the mesolimbic pathway.
-negative symptoms (e.g disorganised thought) may result from hypodopaminergia, a lack of dopaminergic activity in the mesocortiyal pathway.
Excess of dopaminergic activity in what pathway results in positive symptoms?
Mesolimbic
lack of dopaminergic activity in what pathway results in negative symptoms?
mesocortical
Serotonin and negative symptoms
(what does clozapine bind to and how may this lead to symptoms?)
later research focused on the roles of other neurotransmitters (GABA, glutamate and serotonin).
Newer antipsychotic drug (clozapine) binds to D1 and D4 dopamine receptors.
The effectiveness of this drug called into question the original dopamine hypothesis (with its focus on D2 receptors).
Clozapine also binds to serotonin receptors and reduces positive and negative symptoms of schizophrenia - so negative symptoms may be caused by irregular serotonergic activity.
research then focused on the interactions between different neurotransmitters (e.g serotonin regulates dopamine levels in the mesolimbic pathway).
Dopamine dysregulation
How’s and Kapur’s (2009) version of the hypothesis:
-dopamine dysregulation in the Striatum is the common pathway to psychosis (schizophrenia)
-attention should turn to high presynaptic dopamine levels as opposed to irregularities of D2 receptors.
-focus on interactions between genetic, environmental and sociocultural factors.
-Dopamine hypothesis should be softened and viewed as an explanation for ‘psychosis proneness’, not as an explanation specifically for schizophrenia.
who conducted research into a more recent version of the dopamine hypothesis suggesting dopamine dysregulation?
Howes and Kapur (2009)
what does Howes and kapur believe the dopamine hypothesis should be viewed and what do they focus on?
Dopamine hypothesis should be softened and viewed as an explanation for ‘psychosis proneness’, not as an explanation specifically for schizophrenia.
focus on interactions between genetic, environmental and sociocultural factors.
strengths
support from amphetamine-induced psychosis in rats
Tenn et al. (2003) found that rats given nine amphetamine injections over three weeks showed various schizophrenia-like symptoms.
Dopamine antagonists (drugs that block D1 receptors) successfully reversed these effects.
This experimental evidence suggests that increased dopamine levels may be a cause of schizophrenia in symptoms.
Support for the role of D2 receptors.
Snyder (1985) found that chlorpromazine is an antagonist at many dopamine receptors (D1 and D2) and has an antipsychotic effect.
He also found that the dopamine antagonist haloperidol is more effective even though is has a narrower range of biochemical effects.
This finding suggests that excess activity at specific (but not all) dopamine receptors is implicated in development of symptoms.
Name two supporting researchers
Tenn et al. 2003
Snyder 1985